Basic Research
Copyright ©The Author(s) 2002. Published by Baishideng Publishing Group Inc. All rights reserved.
World J Gastroenterol. Oct 15, 2002; 8(5): 918-922
Published online Oct 15, 2002. doi: 10.3748/wjg.v8.i5.918
The pre-synaptic blocker toosendanin does not inhibit secretion in exocrine cells
Zong-Jie Cui, Xue-Hui He
Zong-Jie Cui, Xue-Hui He, Institute of Cell Biology, Beijing Normal University, Beijing 100875, China
Author contributions: All authors contributed equally to the work.
Supported by Natural Science Foundation of China Grant No.39870367, 39825112, 30070286, and The Ph.D. Program of the Ministry of Education, China.
Correspondence to: Zong-Jie Cui, Ph.D. (Cantab.), Professor, Institute of Cell Biology, Beijing Normal University, Beijing 100875, China. zjcui@bnu.edu.cn
Telephone: +86-10-6220 9162 Fax: +86-10-6220 9162
Received: April 18, 2002
Revised: June 4, 2002
Accepted: June 8, 2002
Published online: October 15, 2002
Abstract

AIM: Toosendanin is a pre-synaptic blocker at the neuromuscular junction and its inhibitory effect is divided into an initial facilitative/stimulatory phase followed by a prolonged inhibitory phase. The present study investigated whether the subsequent inhibitory phase was due to exhaustion of the secretory machinery as a result of extensive stimulation during the initial facilitative phase. More specifically, this paper examined whether toosendanin could directly inhibit the secretory machinery in exocrine cells.

METHODS: Rat pancreatic acinar cells were isolated by collagenase digestion. Secretion was assessed by measuring the amount of amylase released into the extracellular medium as a percentage of the total present in the cells before stimulation. Cholecystokinin (CCK)-induced increases in intracellular calcium in single cells were measured with fura-2 microfluorometry.

RESULTS: Effects of toosendanin on CCK-induced amylase secretion and calcium oscillations were investigated. Toosendanin of 87-870 μM had no effect on 10 pM-100 nM CCK-stimulated amylase secretion, nor did 8.7-870 μM toosendanin inhibit 5 pM CCK-induced calcium oscillations. In contrast, 10 nM CCK1 receptor antagonist FK 480 completely blocked 5 pM CCK-induced calcium oscillations.

CONCLUSION: The pre-synaptic "blocker" toosendanin is a selective activator of the voltage-dependent calcium channels, but does not interfere with the secretory machinery itself.

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